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Inappropriate p53 activation during development induces features of CHARGE syndrome

Author

Listed:
  • Jeanine L. Van Nostrand

    (Stanford University School of Medicine)

  • Colleen A. Brady

    (Stanford University School of Medicine
    Present addresses: Cardiovascular Research Center and Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA (C.A.B.); Department of Medicine, University of Central Florida, Orlando, Florida 32827, USA (M.M.K.); Department of Emergency Medicine, Oregon Health and Science University, Portland, Oregon 97239, USA (T.M.J.).)

  • Heiyoun Jung

    (Stanford University School of Medicine)

  • Daniel R. Fuentes

    (Stanford University School of Medicine)

  • Margaret M. Kozak

    (Stanford University School of Medicine
    Present addresses: Cardiovascular Research Center and Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA (C.A.B.); Department of Medicine, University of Central Florida, Orlando, Florida 32827, USA (M.M.K.); Department of Emergency Medicine, Oregon Health and Science University, Portland, Oregon 97239, USA (T.M.J.).)

  • Thomas M. Johnson

    (Stanford University School of Medicine
    Present addresses: Cardiovascular Research Center and Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA (C.A.B.); Department of Medicine, University of Central Florida, Orlando, Florida 32827, USA (M.M.K.); Department of Emergency Medicine, Oregon Health and Science University, Portland, Oregon 97239, USA (T.M.J.).)

  • Chieh-Yu Lin

    (Stanford University School of Medicine)

  • Chien-Jung Lin

    (Stanford University School of Medicine)

  • Donald L. Swiderski

    (The University of Michigan Medical School)

  • Hannes Vogel

    (Stanford University School of Medicine)

  • Jonathan A. Bernstein

    (Stanford University School of Medicine)

  • Tania Attié-Bitach

    (Hôpital Necker-Enfants Malades, APHP
    Unite INSERM U1163, Université Paris Descartes-Sorbonne Paris Cité, Institut Imagine)

  • Ching-Pin Chang

    (Krannert Institute of Cardiology, Indiana University School of Medicine)

  • Joanna Wysocka

    (Stanford University School of Medicine
    Stanford University School of Medicine)

  • Donna M. Martin

    (The University of Michigan Medical School
    The University of Michigan Medical School)

  • Laura D. Attardi

    (Stanford University School of Medicine
    Stanford University School of Medicine)

Abstract

Inappropriate activation of the tumour-suppressor protein p53 during development can promote phenotypes similar to those of CHARGE syndrome, suggesting that p53 activation not only has a beneficial function in suppressing cancer but also a deleterious function in promoting developmental syndromes.

Suggested Citation

  • Jeanine L. Van Nostrand & Colleen A. Brady & Heiyoun Jung & Daniel R. Fuentes & Margaret M. Kozak & Thomas M. Johnson & Chieh-Yu Lin & Chien-Jung Lin & Donald L. Swiderski & Hannes Vogel & Jonathan A., 2014. "Inappropriate p53 activation during development induces features of CHARGE syndrome," Nature, Nature, vol. 514(7521), pages 228-232, October.
  • Handle: RePEc:nat:nature:v:514:y:2014:i:7521:d:10.1038_nature13585
    DOI: 10.1038/nature13585
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    Cited by:

    1. Caojie Liu & Qiuchan Xiong & Qiwen Li & Weimin Lin & Shuang Jiang & Danting Zhang & Yuan Wang & Xiaobo Duan & Ping Gong & Ning Kang, 2022. "CHD7 regulates bone-fat balance by suppressing PPAR-γ signaling," Nature Communications, Nature, vol. 13(1), pages 1-12, December.
    2. Jing Nie & Yoshitomo Ueda & Alexander J. Solivais & Eri Hashino, 2022. "CHD7 regulates otic lineage specification and hair cell differentiation in human inner ear organoids," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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